Obstructive Lung Diseases Overview

Obstructive Lung Diseases

• Obstructive lung diseases involve four main disorders: emphysema, chronic bronchitis, asthma, and bronchiectasis.

Emphysema

• Emphysema is a lung condition characterized by the permanent enlargement of air spaces distal to terminal bronchioles, along with destruction of their walls.
• This occurs without significant fibrosis, reducing the lungs' ability to exchange gases effectively and causing breathing problems.
• Emphysema's damage includes destruction of alveolar air sacs and loss of elastic recoil.

Types of Emphysema

• Centriacinar (centrilobular): Primarily affects central parts of the acini (respiratory bronchioles), sparing distal alveoli. Lesions are more common in the upper lobes, especially apical areas. Frequently occurs in cigarette smokers and associated with chronic bronchitis. Can also affect distal acinus in severe cases.
• Panacinar (panlobular): Uniform enlargement of acini, affecting respiratory bronchioles, alveolar ducts, and terminal alveoli. Predominantly impacts the lower lung zones. Associated with alpha-1 antitrypsin deficiency.
• Distal acinar (paraseptal): Predominantly affects distal parts of the acini, with normal proximal portions. More prominent around the pleura, lobular connective tissue septa, and margins of lobules. Often occurs near fibrotic, scarred, or atelectatic areas and is more severe in the upper half of the lungs. Associated with spontaneous pneumothorax.

Chronic Bronchitis

• A long-term condition defined by a productive cough lasting at least three months in two consecutive years.
• Commonly affects smokers and those in polluted environments (e.g., sulfur dioxide, nitrogen dioxide).
• Key feature: Hypertrophy of mucous glands and increased goblet cells leading to mucus hypersecretion in large airways of the lungs.

Asthma

• A chronic inflammatory disorder of the airways characterized by recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night and/or early morning.
• Involves reversible airway obstruction, increased mucus production, and inflammation primarily involving eosinophils and mast cells.

Bronchiectasis

• Permanent dilation of bronchi and bronchioles caused by destruction of smooth muscle and elastic tissue.
• Typically linked to chronic necrotizing infections.
• It's not a primary disorder, but a secondary result from persistent infection or obstruction caused by various conditions.
• Especially affects the lower lobes bilaterally, targeting vertical air passages.

Pathology Notes

• Reid Index: A measurement of the thickness of the glands and walls of the bronchi to determine the presence of chronic bronchitis. A Reid index above 40% indicates chronic bronchitis.
• Blue Bloater: A clinical presentation of chronic bronchitis, characterized by cyanosis and hypoxia due to poor oxygenation and carbon dioxide retention, often with increased body weight and puffiness.
• Status Asthmaticus: A severe, life-threatening episode of asthma, often requiring emergency medical intervention. In this state, the patient's lungs appear hyper-inflated, distended or distended with air, despite outward appearance.
• Atopic Asthma: The most common type, characterized by IgE-mediated hypersensitivity to allergens. Triggers include allergens (dust, pollen, animal dander, food) and respiratory infections. Begins consistently during childhood and often has a family history.
• Non-Atopic Asthma: Asthma without evidence of allergen sensitization. Triggers include viral respiratory infections and inhaled pollutants. May be triggered by viral inflammation within respiratory mucosa, reducing the threshold to irritants.
• Occupational Asthma: Asthma triggered by exposure to specific antigens in the workplace. Common causes include fumes (e.g., epoxy resins), organic dusts (e.g., wood, cotton), and chemicals (e.g., toluene).
• Airway Remodeling: Structural changes in bronchial walls as a result of repeated inflammation, including thickening of walls, increased smooth muscle and collagen deposition, mucus hypersecretion, epithelial cell changes, airway narrowing, and vascular changes.
• Morphology:
  -Curschmann Spirals: Dense, tenacious mucus plugs with shed epithelium whorls in asthma and often associated with airway plugging.
  • Charcot-Leyden Crystals: Crystalloids made up of eosinophil protein galectin-10, found in asthma.
  • Bronchioles/Bronchi Dilation: Dilation occurring in bronchiectasis, stretching up to four times normal diameter and often visible reaching to the pleural surface.

Pathogenesis

• Emphysema: Protease-anti-protease imbalance, oxidative stress, and inflammatory cells are key factors. Smoking and genetic conditions can contribute.
• Chronic Bronchitis: Environmental irritants cause inflammation, with macrophages, neutrophils, and lymphocytes infiltrating the airways. Inflammatory mediators, and cytokine mediators exacerbate the issue.
• Asthma: Activation of Type 2 Helper T (TH2) cells triggers cytokine production leading to IgE antibody production, mast cell activation and release of mediators like histamine, leukotrienes, and prostaglandins. Eosinophil activation and mucus production further exacerbate the narrowing of the airways. -Bronchiectasis: Chronic inflammation and infection damage the smooth muscle and elastic tissue of bronchi and bronchioles, causing lasting dilation of the affected airways. Infection is the leading cause.